PMID- 24750267 OWN - NLM STAT- MEDLINE DCOM- 20150930 LR - 20211021 IS - 1939-1676 (Electronic) IS - 0891-6640 (Print) IS - 0891-6640 (Linking) VI - 28 IP - 4 DP - 2014 Jul-Aug TI - Effect of dietary nonstructural carbohydrate content on activation of 5'-adenosine monophosphate-activated protein kinase in liver, skeletal muscle, and digital laminae of lean and obese ponies. PG - 1280-8 LID - 10.1111/jvim.12356 [doi] AB - BACKGROUND: In EMS-associated laminitis, laminar failure may occur in response to energy failure related to insulin resistance (IR) or to the effect of hyperinsulinemia on laminar tissue. 5'-Adenosine-monophosphate-activated protein kinase (AMPK) is a marker of tissue energy deprivation, which may occur in IR. HYPOTHESIS/OBJECTIVES: To characterize tissue AMPK regulation in ponies subjected to a dietary carbohydrate (CHO) challenge. ANIMALS: Twenty-two mixed-breed ponies. METHODS: Immunohistochemistry and immunoblotting for total AMPK and phospho(P)-AMPK and RT-qPCR for AMPK-responsive genes were performed on laminar, liver, and skeletal muscle samples collected after a 7-day feeding protocol in which ponies stratified on body condition score (BCS; obese or lean) were fed either a low-CHO diet (ESC + starch, approximately 7% DM; n = 5 obese, 5 lean) or a high-CHO diet (ESC + starch, approximately 42% DM; n = 6 obese, 6 lean). RESULTS: 5'-Adenosine-monophosphate-activated protein kinase was immunolocalized to laminar keratinocytes, dermal constituents, and hepatocytes. A high-CHO diet resulted in significantly decreased laminar [P-AMPK] in lean ponies (P = .03), but no changes in skeletal muscle (lean, P = .33; obese, P = .43) or liver (lean, P = .84; obese, P = .13) [P-AMPK]. An inverse correlation existed between [blood glucose] and laminar [P-AMPK] in obese ponies on a high-CHO diet. CONCLUSIONS AND CLINICAL IMPORTANCE: Laminar tissue exhibited a normal response to a high-CHO diet (decreased [P-AMPK]), whereas this response was not observed in liver and skeletal muscle in both lean (skeletal muscle, P = .33; liver, P = .84) and obese (skeletal muscle, P = .43; liver, P = .13) ponies. CI - Copyright (c) 2014 by the American College of Veterinary Internal Medicine. FAU - Burns, T A AU - Burns TA AD - The Ohio State University College of Veterinary Medicine, Columbus, OH. FAU - Watts, M R AU - Watts MR FAU - Weber, P S AU - Weber PS FAU - McCutcheon, L J AU - McCutcheon LJ FAU - Geor, R J AU - Geor RJ FAU - Belknap, J K AU - Belknap JK LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20140420 PL - United States TA - J Vet Intern Med JT - Journal of veterinary internal medicine JID - 8708660 RN - 0 (Blood Glucose) RN - 0 (Dietary Carbohydrates) RN - 0 (Insulin) RN - EC 2.7.11.31 (AMP-Activated Protein Kinases) SB - IM MH - AMP-Activated Protein Kinases/*metabolism MH - Animals MH - Blood Glucose/analysis MH - Blotting, Western/veterinary MH - Dietary Carbohydrates/*pharmacology MH - Enzyme Activation/drug effects MH - Hoof and Claw/drug effects/*enzymology MH - Horse Diseases/*enzymology/metabolism MH - Horses MH - Insulin/blood MH - Liver/drug effects/*enzymology MH - Muscle, Skeletal/drug effects/*enzymology MH - Obesity/enzymology/metabolism/*veterinary MH - Real-Time Polymerase Chain Reaction/veterinary MH - Thinness/enzymology/metabolism/*veterinary PMC - PMC4857936 OTO - NOTNLM OT - Energy regulation OT - Equine metabolic syndrome OT - Insulin resistance OT - Laminitis EDAT- 2014/04/23 06:00 MHDA- 2015/10/01 06:00 PMCR- 2014/07/01 CRDT- 2014/04/23 06:00 PHST- 2013/08/15 00:00 [received] PHST- 2013/12/13 00:00 [revised] PHST- 2014/03/05 00:00 [accepted] PHST- 2014/04/23 06:00 [entrez] PHST- 2014/04/23 06:00 [pubmed] PHST- 2015/10/01 06:00 [medline] PHST- 2014/07/01 00:00 [pmc-release] AID - JVIM12356 [pii] AID - 10.1111/jvim.12356 [doi] PST - ppublish SO - J Vet Intern Med. 2014 Jul-Aug;28(4):1280-8. doi: 10.1111/jvim.12356. Epub 2014 Apr 20.